Transgenically ectopic expression of Bmp4 to the Msx1 mutant dental mesenchyme restores downstream gene expression but represses Shh and Bmp2 in the enamel knot of wild type tooth germ
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Abstract
Bmp4 is a downstream gene of Msx1 in early mouse tooth development. In this study,
we introduced the Msx1-Bmp4 transgenic allele to the Msx1 mutants in which tooth development
is arrested at the bud stage in an effort of rescuing Msx1 mutant tooth phenotype
in vivo. Ectopic expression of a Bmp4 transgene driven by the mouse Msx1promoter in
the dental mesenchyme restored the expression of Lef-1 and Dlx2 but neither Fgf3 nor
syndecan-1 in the Msx1 mutant molar tooth germ. The mutant phenotype of molar but
not incisor could be partially rescued to progress to the cap stage. The Msx1-Bmp4
transgene was also able to rescue the alveolar processes and the neonatal lethality
of the Msx1 mutants. In contrast, overexpression of Bmp4 in the wild type molar mesenchyme
down-regulated Shh and Bmp2 expression in the enamel knot, the putative signaling
center for tooth patterning, but did not produce a tooth phenotype. These results
indicate that Bmp4 can bypass Msx1 function to partially rescue molar tooth development
in vivo, and to support alveolar process formation. Expression of Shh and Bmp2 in
the enamel knot may not represent critical signals for tooth patterning.